Additionally, sEH genetic deletion alleviated the course of Cis-induced AKI and abolished the reno-protective effect of alisol B in Cis-induced AKI mice, revealing that the inhibition of sEH by alisol B to enhance the level of EETs resulted in its renal protective effect through the regulation of apoptosis, oxidative stress, and inflammation. Here, EPHX2 is linked to acute kidney injury.